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SM Neuro Flashcards

1
Q

A patient is experiencing decreased hearing in the right ear. The NP completes both the Rinne and Weber tests. If the patient has Meniere disease, what would be the expected finding on the Weber test?
1. Air conduction is two times longer than bone conduction
2. Bone conduction is two times longer than air conduction
3. The tuning fork sound lateralizes to the right ear
4. The tuning fork sound lateralizes to the left ear

A

4.

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2
Q

sx of a brain tumor HA

A

dull persistent HA; always in same spot; accompanied (or not) by N/V, visual disturbances, behavioral changes

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3
Q

S/S of a red flag HA

A

Thunderclap HA
“Worst HA of my life”

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4
Q

what imaging technique can be used to quickly rule out stroke?

A

CT

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5
Q

what are the classic sx of stroke?

A

unilateral weakness, facial drooping, slurred speech

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6
Q

what is treatment for stroke based on?

A

type of stroke

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7
Q

what are the two main types of stroke?

A

hemorrhagic
ischemic

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8
Q

does HTN increase risk for hemorrhagic or ischemic stroke?

A

hemorrhagic

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9
Q

does atrial fibrillation increase the risk for hemorrhagic or ischemic stroke?

A

ischemic

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10
Q

how do you differentiate a TIA from a stroke?

A

sx are identical at first, but sx resolve w/i 24 hours (most often w/i 1 hr of onset)

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11
Q

what does the acronym BE FAST relate to? what does it stand for?

A

sx of stroke
Balance, Eyes, Face, Arm, Speech, Time

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12
Q

what are the areas of the brain impacted by stroke?

A

Wernicke’s area
Broca’s area

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13
Q

if a stroke affects the Wernicke area of brain, what sx result?

A

receptive aphasia - patient cannot understand what is being said to them
-no longer receptive to that information
*R and W are close together in alphabet

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14
Q

if a stroke affects the Broca area of brain, what sx result?

A

expressive aphasia - patient has trouble expressing themselves or forming speech
*B and E are close together in the alphabet

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15
Q

-in what population is Wernicke-Korsakoff syndrome present?
-what vitamin is this population depleted of?
*what can low levels of this vitamin lead to?

A

-common in those who use alcohol excessively
-vitamin B-1 (thiamin)
-can lead to damage to both the thalamus and hypothalamus causing confusion, ataxia, and vision abnormalities

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16
Q

Type of HA:
Unilateral HA, tearing up/runny nose, occurs same time everyday

A

Cluster HA

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17
Q

tx for cluster HA

A

100% O2, CCBs

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18
Q

Type of HA:
Unilateral HA, possible visual impairment, temple pain/pulsing, increased ESR
-can cause HA, jaw pain, vision changes, can result in permanent blindness
-pain can come and go, but very severe in nature

A

Giant Cell Arteritis (Temporal Arteritis)

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19
Q

what are the sx of giant cell arteritis?

A

Unilateral HA, possible visual impairment, temple pain/pulsing, increased ESR
-can cause HA, jaw pain, vision changes, can result in permanent blindness
-pain can come and go, but very severe in nature

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20
Q

tx for giant cell arteritis

A

long-term high dose steroids

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21
Q

how do you diagnose giant cell arteritis?

A

temporal artery biopsy

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22
Q

is giant cell arteritis managed in primary care?

A

no; refer!

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23
Q

a patient with giant cell arteritis is being referred
-what must we as the primary care provider ensure takes place regardless of referral?

A

do not delay starting steroids (long-term high dose steroids)

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24
Q

what can temporal arteritis lead to?

A

permanent blindness

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25
Q

Type of HA:
occipital HA, typically upon awakening; unilateral

A

HTN HA

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26
Q

tx for HTN HA

A

evaluate BP management

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27
Q

Type of HA:
throbbing, pulsing HA; possible N/V, sensitive to lights or noise; aura; unilateral

A

migraine

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28
Q

Type of HA:
bilateral HA; typically presents with throbbing bilaterally; pressure/tight band

A

tension HA

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29
Q

what is commonly associated with temporal arteritis?

A

polymyalgia rheumatica

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30
Q

what is commonly associated with polymyalgia rheumatica?

A

temporal arteritis

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31
Q

sx associated with polymyalgia rheumatica

A

-inflammatory disorder
-causes increased muscle pain
-increased inflammatory markers

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32
Q

typical prophylaxis for migraine HA

A

-avoid triggers
-can use betablockers (propranolol); TCA (amitriptyline), anti-epileptic (topiramate = Topamax)

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33
Q

abortive tx for migraine HA (ie)

A

triptan drug class is mainstay ie sumatriptan (imitrex)

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34
Q

what population cannot be prescribed a triptan drug for migraine HA abortive tx?

A

pts with uncontrolled HTN and those on other serotonin meds (SSRI)
-can lead to increased risk of serotonin syndrome

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35
Q

pathophysiology of Parkinson’s disease

A

decreased dopamine leads to degradation of basal ganglia leading to progressive sx affecting the NS

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36
Q

what neurotransmitter is depleted in those dx with Parkinson’s disease?

A

dopamine

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37
Q

typical tx for Parkinson’s disease

A

levadopa/carbidopa = Sinemet

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38
Q

what happens if Parkinson med Sinemet is taken for long period of time?

A

it stops working for Parkinson sx (ineffective)

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39
Q

symptoms of Parkinson’s disease

A

-bradykinesia (most debilitating, overall)
-resting tremor
-rigidity
-postural instability (impairments in gate or balance)

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40
Q

what disease does Brudzinski sign help to dx?

A

meningitis

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41
Q

what disease dose Kernig sign help to dx?

A

meningitis

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42
Q

what is the Brudzinski sign?

A

when flexing (passive flexion of neck) back of head, causes hips and knees to flex with it d/t meningeal irritation

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43
Q

what is the Kernig sign?

A

patient cannot extend their knee passing 90 degree angle without pain
-Kernig – Knee

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44
Q

what diagnostic test is conducted if either the Brudzinski or Kernig sign is positive?

A

refer for emergent spinal tap and admission

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45
Q

what characterizes multiple sclerosis?

A

chronic condition that affects NS characterized by demyelinated lesions in the brain
-causes scaring in brain; affects communication to peripheral nerves

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46
Q

sx of MS

A

weakness, sensory loss, fatigue; vision loss if optic nerve impacted

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47
Q

tx for MS

A

no cure; tx aimed at slowing disease progression

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48
Q

goal of Alzheimer’s disease tx

A

no cure; tx aids to slow progression of overall loss of cognitive fx

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49
Q

3 A’s of Alzheimer’s disease

A
  1. Apraxia: inability to carry out movements or gestures
  2. Agnosia: inability to recognize familiar faces/people
  3. Aphasia: inability to comprehend things ie reading, writing, expression by others
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50
Q

what does apraxia mean?

A

inability to carry out movements or gestures

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51
Q

what does agnosia mean?

A

inability to recognize familiar faces/people

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52
Q

what does aphasia mean?

A

inability to comprehend things ie reading, writing, expression by others

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53
Q

what quick assessment tool is used to assess cognitive fx/decline and possible dementia?

A

Mini Mental Status Exam (MMSE)

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54
Q

Order of cranial nerves (what roman numeral):
olfactory

A

I

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55
Q

Order of cranial nerves (what roman numeral):
optic

A

II

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56
Q

Order of cranial nerves (what roman numeral):
occulomotor

A

III

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57
Q

Order of cranial nerves (what roman numeral):
trochlear

A

IV

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58
Q

Order of cranial nerves (what roman numeral):
trigeminal

A

V

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59
Q

Order of cranial nerves (what roman numeral):
Abducens

A

VI

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60
Q

Order of cranial nerves (what roman numeral):
Facial

A

VII

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61
Q

Order of cranial nerves (what roman numeral):
Vestibulocochlear

A

VIII

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62
Q

Order of cranial nerves (what roman numeral):
Glossopharyngeal

A

IX

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63
Q

Order of cranial nerves (what roman numeral):
Vagus

A

X

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64
Q

Order of cranial nerves (what roman numeral):
Accessory

A

XI

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65
Q

Order of cranial nerves (what roman numeral):
Hypoglossal

A

XII

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66
Q

what is the name of this cranial nerve?
I

A

olfactory

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67
Q

what is the name of this cranial nerve?
II

A

optic

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68
Q

what is the name of this cranial nerve?
III

A

occulomotor

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69
Q

what is the name of this cranial nerve?
IV

A

Trochlear

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70
Q

what is the name of this cranial nerve?
V

A

Trigeminal

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71
Q

what is the name of this cranial nerve?
IV

A

Abducens

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72
Q

what is the name of this cranial nerve?
VII

A

Facial

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73
Q

what is the name of this cranial nerve?
VIII

A

Vestibulocochlear

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74
Q

what is the name of this cranial nerve?
IX

A

Glossopharyngeal

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75
Q

what is the name of this cranial nerve?
X

A

Vagus

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76
Q

what is the name of this cranial nerve?
XI

A

Accessory

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77
Q

what is the name of this cranial nerve?
XII

A

Hypoglossal

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78
Q

what is the phrase to help us remember all the cranial nerves (in order)?

A

Oh, Oh, Oh To Touch And Feel A Great Vein - Ah, Heaven!

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79
Q

Is this cranial nerve sensory, motor, or both?
Olfactory

A

Sensory

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80
Q

Is this cranial nerve sensory, motor, or both?
Optic

A

Sensory

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81
Q

Is this cranial nerve sensory, motor, or both?
Occulomotor

A

Motor

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82
Q

Is this cranial nerve sensory, motor, or both?
Trochlear

A

Motor

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83
Q

Is this cranial nerve sensory, motor, or both?
Trigeminal

A

Both

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84
Q

Is this cranial nerve sensory, motor, or both?
Abducens

A

Motor

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85
Q

Is this cranial nerve sensory, motor, or both?
Facial

A

Both

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86
Q

Is this cranial nerve sensory, motor, or both?
Vestibulocochlear

A

Sensory

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87
Q

Is this cranial nerve sensory, motor, or both?
Glossopharyngeal

A

Both

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88
Q

Is this cranial nerve sensory, motor, or both?
Vagus

A

Both

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89
Q

Is this cranial nerve sensory, motor, or both?
Accessory

A

Motor

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90
Q

Is this cranial nerve sensory, motor, or both?
Hypoglossal

A

Motor

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91
Q

what is the phrase to help us remember if the cranial nerves are sensory, motor, or both (in order)?

A

Some Say Marry Money But My Brother Says Big Brains Matter More

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92
Q

symptoms of trigeminal neuralgia

A

severe, stabbing pain in face down one or more of the three branches of the trigeminal nerve

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93
Q

tx for trigeminal neuralgia

A

Tegretol (most common; but there are other tx)

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94
Q

what is a medication that treats trigeminal neuralgia?

A

Tegretol

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95
Q

what are patients at increased risk for if trigeminal neuralgia pain is not under control?

A

increased risk of suicide

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96
Q

what cranial nerve is affected during Bell’s Palsy?

A

CN VII

97
Q

what does every patient need to utilize if diagnosed with Bell’s Palsy?

A

eye lubricant

98
Q

why do Bell’s Palsy pts need to utilize eye lubricant?

A

decreased risk of corneal abrasion

99
Q

what tests are used to assess CN VIII (vestibulocochlear)?

A

Rinne test
Weber test

100
Q

what cranial nerve does the Rinne test examine?

A

CN VIII (vestibulocochlear)

101
Q

what cranial nerve does the Weber test examine?

A

CN VIII (vestibulocochlear)

102
Q

process of the Rinne test

A

-strike tuning fork and place under pinna which is on the mastoid bump (initial location)
-once patient doesn’t hear sound anymore, move tuning fork directly next to ear and see how much longer they hear it

103
Q

normal result of Rinne test

A

air conduction is going to be two times longer than bone conduction when utilizing tuning fork
*A comes before B
*Air longer than Bone

104
Q

abnormal result of Rinne test

A

bone conduction is longer than air conduction

105
Q

process of Weber test

A

after striking, place tuning fork on top of head

106
Q

normal result of Weber test

A

sound will be heard equally by BOTH ears (there is no lateralization)

107
Q

-abnormal results of Weber test
-once abnormal result obtained, what must be concluded next?

A
  1. lateralize to unaffected ear
  2. lateralize to affected or bad ear
    -conductive or sensorineural hearing loss
108
Q

conductive hearing loss (Weber test)

A

-sound of Weber Test will lateralize to the bad ear (affected ear)
*noise heard louder in ear pt currently has issues with
-this issue can be seen physically: cholesteatoma; cerumen impaction

109
Q

sensorineural hearing loss (Weber test)

A

-sound from Weber test is going to lateralize to patient’s good or unaffected ear
-this issue cannot be seen physically: Meniere’s disease, age, medication

110
Q

what is cholesteatoma?

A

collection of skin cells within the ear; can often cause large mass in inner ear that needs surgical removal

111
Q

-what is otosclerosis?
*is it conductive or sensorineural hearing loss?

A

bones in middle ear become struck in place and they no longer vibrate
-issue we can see (in the middle ear) = conductive hearing loss

112
Q

sx of Meniere disease
-what is our biggest concern?

A

typical presentation: vertigo, tinnitus, ear pressure; common to see nystagmus
-potential permanent hearing loss d/t degradation of cochlea, which is responsible for relaying sounds to the brain for hearing

113
Q

pathophysiology of Meniere disease

A

abnormality of the inner ear labyrinth –> leads to vertigo and hearing loss

114
Q

what are the two types of migraines?

A

Migraines without aura
Migraines with aura

115
Q

common S/S of migraine (6)

A

possible aura
unilateral
throbbing HA behind eyes
N/V
photophobia
phonophobia

116
Q

what is an aura?

A

sensory disturbance that typically precedes or occurs during the HA itself

117
Q

how long can migraines last?

A

couple of hours to three days; disruptive to normal life and function

118
Q

characteristics of migraine w/o aura

A

-at least 5 HA/MO lasting 4-72hrs
-two of the following:
*unilateral
*pulsating
*moderate/severe intensity
*aggravation by or avoidance of regular physical activity
-in addition, at least one or the following:
*N/V
*photophobia/phonophobia

119
Q

characteristics of migraine w/ aura

A

-at least 2 HA/MO lasting 4-72hrs
-two of the following:
*unilateral
*pulsating
*moderate/severe intensity
*aggravation by or avoidance of regular physical activity
-in addition, at least one or the following:
*N/V
*photophobia/phonophobia
-clear description of how aura presented

120
Q

medication management of migraines: prophylactic medication classes

A

-Beta blockers (mainstay therapy)
-TCA (ie amitriptyline)
-Anti-epileptic (topiramate (topamax), valproic acid (depakote)

121
Q

what is the mainstay therapy for prophylactic pharmacologic treatment for migraine HA?

A

beta blockers

122
Q

when is a prophylactic medication prescribed to migraine patient?

A

when patient is having significant disruption in day-to-day life ie 4 or more HA per MO or taking abortive meds >2x weekly

123
Q

when should an abortive therapy be taken by a migraine patient?

A

as soon as patient recognizes HA is occurring

124
Q

abortive medications for migraine:
-mild sx
-more severe sx

A

-combination analgesics (aspirin, caffeine, acetaminophen); NSAIDs frequently utilized
-“triptan” ie sumatriptan (Imitrex)

125
Q

what patients cannot receive sumatriptan (Imitrex)?

A

patients with CAD or uncontrolled HTN

126
Q

what should the provider consider ordering for a patient with cardiac issues when trying to prescribe triptans?

A

ECG

127
Q

if a “triptan” medication ie sumatriptan does not help patient with migraines, can other drugs from same class be used?

A

Yes
-can often see efficacy with another drug from same class (can switch meds w/i same class as needed to control pt sx)

128
Q

what is the highest risk factor for giant cell arteritis?

A

age
-tends to occur more as people age (often btw 70-80YO)

129
Q

sx of giant cell arteritis?

A

-unilateral HA; near temporal region of face
-stereotypical to present with “cord like” temporal artery; warm and tender to the touch
-jaw claudication (pain while chewing)
-vision loss

130
Q

what is a concerning symptoms of temporal arteritis?

A

-vision loss –> can become permanent

131
Q

things to consider when treating temporal arteritis (how quickly; what is tx?)

A

-must treat ASAP –> even before diagnostics come back
-high potency steroids

132
Q

how is giant cell arteritis diagnosed?

A

-inflammatory markers: ESR, CRP (almost always elevated in this condition; not used to make definitive diagnosis)
-temporal artery diagnosis (for definitive dx)

133
Q

-what is polymyalgia rheumatica?
-what condition tends to coincide with polymyalgia rheumatica?

A

-highly inflammatory condition; pain in large muscle groups of the body
-giant cell arteritis

134
Q

-what is the treatment for temporal arteritis?
-how is treatment altered if visual loss is a sx?
-how long are patients on treatment?
-how quickly do sx resolve on treatment?

A

-long-term, high dose steroids
-utilize even higher doses of steroids and REFER TO ED
-1-2 years and then will gradually taper down
-quickly!

135
Q

symptoms of cluster headache

A

-sudden, sharp, unilateral HA behind eye
-severe HA
-more common in males
-common to see nasal drainage and tearing
-may suffer from multiple attacks in the same week
-last minutes to hours in duration
-can be associated w/ alc/tobacco use; pts tend to be restless in nature and diaphoretic

136
Q

what type of headache do these sx describe?
-sudden, sharp, severe
-unilateral
-common to see nasal drainage and tearing
-last minutes to hours; multiple attacks per week

A

-cluster HA

137
Q

how are cluster HA diagnosed?

A

no dx tool; based on sx/presentation

138
Q

treatment for cluster HA

A
  1. prophylactic
    -CCB (ie Verapamil (Verelan)) is the gold standard
    *CCB help vasodilate; can cause some HA sx but MAO is totally different
  2. abortive
    -sumatriptan (injection) + high flow O2 100% at 7-15L for 20min; can use intranasal lidocaine
139
Q

what is the prophylactic treatment for cluster HA?

A

CCB - Verapamil (Verelan)

140
Q

what is the abortive treatment for cluster HA?

A

-sumatriptan (injection)
-high flow O2 at 100% 7-15L for 20 min
-intranasal lidocaine

141
Q

what type of HA can increase risk of suicide?

A

cluster HA (d/t severe sx)

142
Q

sx of stroke

A

-“thunderclap HA”
-worst HA of life

143
Q

what does the acronym BE FAST stand for?

A

Balance
Eyes
Face
Arms
Speech
Time

144
Q

-what diagnostics tests are used for stroke?
-why?

A

-CT
-can determine hemorrhagic or ischemic (CT’s are good at seeing hemorrhage in the brain)

145
Q

TIA
-def
-traditionally d/t what?
-what do sx mimic?
-how long do sx last (typically)?
-what is patient at high risk for?

A

-intermittent disruption of brain’s blood supply; only a temporary disruption
-clot
-stroke
-typically 1 hr; patient expected to return to normal w/i 24 hours
-stroke!

146
Q

what is the difference between TIA and stroke?

A

-stroke sx don’t resolve until stroke is treated; some sx linger
*stroke has residual effects:
receptive aphasia (Wenicke’s aphasia)
expressive aphasia (Broca’s aphasia)
-TIA sx typically resolve in 1 hr (expected to return to normal w/i 24 hours)

147
Q

what is Wernicke’s aphasia?

A

can’t comprehend what is said to them
-type of receptive aphasia

148
Q

what is Broca’s aphasia?

A

can’t express thoughts and language; often garbled or incoherent
-type of expressive aphasia

149
Q

what diagnostic test is used for Bell’s Palsy?

A

no dx test; use clinical presentation

150
Q

-sx of Bell’s Palsy
-what cranial nerve is affected?

A

-one-sided facial paralysis (sometimes eye won’t shut); drooling, altered taste (sx range mild to severe)
-CN VII (facial)

151
Q

what should be ruled out with presentation of Bell’s Palsy?

A

Lyme’s disease

152
Q

what is the cause of Bell’s Palsy?

A

unknown
-possible viral infection w/ remissions and exacerbations
-stress, pregnancy, HTN, Pre-E, DM, resp conditions, obesity –> can all be precipitating factors

153
Q

tx for Bell’s Palsy

A

-understand personal triggers
-start steroids w/i 72 hours of sx onset
-antivirals may be utilized depending on pt
-lubricating eye drops or ointment to protect cornea

154
Q

how quickly should steroids be started for a patient diagnosed with Bell’s Palsy?

A

within 72 hours

155
Q

what diagnostic test is used for corneal abrasion?

A

Fluorescein staining

156
Q

what are the differential dx for Bell’s Palsy?

A

cerebral infarction, facial nerve trauma

157
Q

how does sarcoidosis present differently than Bell’s Palsy?

A

sarcoidosis has facial paralysis bilaterally

158
Q

what causes the sx of Parkinson’s disease?

A

depletion of dopamine

159
Q

what are the 4 core sx of Parkinson’s disease?

A
  1. Bradykinesia
  2. Rigidity
  3. Resting tremor
  4. Postural instability
160
Q

Core sx of Parkinson’s Disease: bradykinesia
-def

A

-inability to do find motor tasks ie zip up jacket or less arm swinging while walking
-slowing of patient’s movements: shuffling propulsive gait

161
Q

what core sx of Parkinson’s disease must be present for dx?

A

bradykinesia

162
Q

Core sx of Parkinson’s Disease: rigidity
-def

A

muscles become inflexible, stiff and tight over time

163
Q

Core sx of Parkinson’s Disease: resting tremor
-def

A

tremor that occurs even when patient is at ease/resting

164
Q

Core sx of Parkinson’s Disease: postural instability
-def

A

decreased ability to prevent falls d/t instability and even a freezing gait (usually a later finding)

165
Q

does an essential tremor occur with intent or rest?

A

intent

166
Q

does a Parkinson’s tremor occur with intent or rest?

A

rest

167
Q

how is an essential tremor managed (tx)?

A

-BB like propranolol (Inderal)
-regular physical activity
-botulinum toxin (Botox) injections
-severe cases: treated w/ deep brain stimulation, but rarely

168
Q

what things worsen essential tremors?

A

sexual excitement, nicotine and caffeine worsen

169
Q

how are the symptoms of Parkinson’s disease treated?

A
  1. dopamine agonists ie Ropinirole (Requip)
    -helps w/ motor sx ie tremor and rigidity
  2. levadopa/carbidopa (Sinemet)
    -better control over bradykinesia but want to delay using due to wearing off phenomenon
170
Q

how long after starting levodopa/carbidopa medication will the patient start to experience the wearing off phenomenon?

A

3-5 years

171
Q

can dopamine agonists and levadopa/carbidopa be taken together?

A

yes, or separate.

172
Q

concussion definition

A

traumatic head injury when brain tissue is rocked, causing impact against the skull

173
Q

mild concussion:
-sx
-tx

A

-sleepiness, HA, confusion, dizziness; mostly self-resolving; often requires impact testing and clearance to return to school and sports
-rest, dec screen time, slowly return to normal activity; if pt returns too quickly, can cause worsening of sx

174
Q

severe concussion:
-sx
-managed inpatient or outpatient?
-possible tx

A

-hypoxia, internal bleeding, death
-inpatient
-phenobarbital to prevent seizure activity from the brain injury

175
Q

what is a patient at risk for after having a concussion?

A

another concussion

176
Q

MS
-definition
-age group
-course of disease

A

-demyelination of brain and spinal cord
-20-40
-very unpredictable in nature: go through remissions, exacerbations of sx ie muscle weakness, balance issues, immense fatigue, bladder/bowel incontinence, vision problems

177
Q

what is a common presentation of MS?

A

vision problems d/t communication to optic nerve being affected

178
Q

once diagnosed with MS, what are patients at high risk for?

A

other conditions: ie trigeminal neuralgia, optic neuritis, nystagmus, periphlebitis

179
Q

tx for MS

A

not managed in primary care; referred to neuro
-steroids, DMT (disease modifying therapies)

180
Q

what is optic neuritis?

A

loss of vision in one eye, pain, reduced color vision, blurred vision, reduction of visual acuity
-related to MS (pt at higher risk for other conditions)

181
Q

Meningitis
-def
-what can cause this infection?

A

-inflammation of protective membranes and fluid or meninges that surround brain and spinal cord
-bacteria, virus, parasite

182
Q

what are some complications of meningitis?

A

seizures, hearing loss, memory difficulty, potential future learning disabilities, death (if not appropriately treated)

183
Q

early S/S of meningitis

A

starting to feel ill; may mimic conditions like the flu (fever, fatigue, body aches)

184
Q

later S/S of meningitis

A

pt gets sicker; may see confusion, difficulty walking, skin rash, vomiting; severe unrelenting HA, extremely stiff neck, N, photophobia, dec appetite

185
Q

how is meningitis diagnosed?

A

-Kernig’s sign
-Brudzinski’s sign
-confirm dx with lumbar punction

186
Q

what is the Kernig sign? what does it help to dx?

A

-lie on back, lift and straighten a bent let (90deg to 180deg); positive findings = severe stiffness in hamstrings causes inability to straighten leg when hip is flexed at 90deg
-meningitis

187
Q

what is the Brudzinski sign? what does it help to dx?

A

-lie on back, flex neck (chin to chest); positive findings = instinctively patient will flex hips and knees due to stiffness

188
Q

what causes the Kernig and Brudzinski signs to occur?

A

inflammation in brain and spinal cord; meningitis

189
Q

R/F associated with meningitis

A

-vaccination status
-population that lives in community based dwellings (college students)

190
Q

are patients dx with meningitis managed inpatient or outpatient?

A

inpatient
-IV abx, IV fluids, close monitoring

191
Q

what type of seizure:
commonly dx in childhood; can last 20-30 sec, may appear as if child is daydreaming (blankly stare); traditionally last 10-15 sec

A

absence seizure

192
Q

what are the sx of absence seizures?
(recollection of incidence?)

A

commonly dx in childhood; can last 20-30 sec, may appear as if child is daydreaming (blankly stare); traditionally last 10-15 sec
-some pts flutter eyelids or other small movements (finger rubbing, eye fluttering, chewing motions)
-no recollection

193
Q

how are absence seizures diagnosed?

A

EEG
-triggers often used: sleep deprivation, flashing lights, to try and elicit these seizures during scan

194
Q

what is the hardest type of seizure to capture on EEG?

A

absence seizure

195
Q

do patients outgrow absence seizures?

A

yes, they tend to

196
Q

tx of absence seizures

A

-anti-seizure meds
-ethosuximide (Zarontin)
-Valproic acid (Depakote)
-Lamotrigine (Lamictal)

197
Q

what is the preferred medication for treatment used for absence seizures?

A

ethosuximide (Zarontin)

198
Q

what is ethosuximide (Zarontin) used to treat?

A

absence seizures

199
Q

Tonic-clonic seizures
-def
-education
-length of seizure
-recollect?

A

-convulsion seizure; gran mal (tonic (stiffening), then clonic (convulsing))
-lie patient down, turn on side to avoid aspiration (put nothing into the mouth)
-about 3 min; call 911 if seizure > 5min
-no recollection of seizure

200
Q

treatment for tonic-clonic seizure (4)

A

-valproic acid (Depakote)
-Lamotrigine (Lamictal)
-Topamax (Topiramate)
-Levetiracetam (Keppra)

201
Q

are seizures treated inpatient or outpatient?

A

outpatient while working closely with neurology

202
Q

anticonvulsant medications

A

valproic acid
phenytoin
carbamazepine (tegretol)
gabapentin (Neurontin)

203
Q

Valproic acid
-what is it used to treat?
-what are the SE?
-contraindications

A

-prevent and tx seizures; can be used alone for absence and complex partial seizures; can be used in combo with other meds to tx other seizure types
-affects appetite, metabolism (common to report weight again 10-15lb in first year), gradual hair loss with long-term (4-6MO) therapy (usually dose related)
-do not prescribe to pts with liver complications (fatal hepatotoxicity esp when doses >100mcg)
-do not prescribe to pregnant pts or those who intend on becoming pregnant

204
Q

Valproic acid
-what tests should be monitored if patient is prescribed this med? how often?

A

-monitor liver function tests closely and continue to monitor levels until stable and every so often after that

205
Q

Phenytoin (Dilantin)
-what type of drug is this?
-what does it treat?
-used alone or in combo?
-complications
-contraindications

A

-anticonvulsant
-generalized and complex partial seizures
-alone or in combo w/ other seizure meds
-gingival hyperplasia and hirsutism; can dec effectiveness in birth control
-do not prescribe to pts with liver issues (can be toxic to liver)
*monitor liver function tests

206
Q

Carbamazepine (Tegretol)
-what type of drug is this?
-what is this commonly used to tx?
-how does this drug work?
-within what population is this a good medication to use?
-R/F, subsequent blood work

A

-anti-convulsant
-trigeminal neuralgia
-lessen pain signals sent to brain; mildly anticholinergic
-elderly (only mildly anticholinergic)
-risk for bone marrow suppression and agranulocytosis; order CBC prior to initiating med and q 3 MO for first year while taking

207
Q

what are patients at risk for when taking carbamazepine (Tegretol)?

A

bone marrow suppression and agranulocytosis

208
Q

Gabapentin (Neurontin)
-what type of medication is this?
-what is it commonly used for?
-patho
-very important characteristic of this med!!!
-SE

A

-anticonvulsant
-tx of peripheral neuropathy and postherpetic neuralgia (nerve pain/tingling that occurs after shingles outbreak)
-works in brain by altering electrical activity and working on neurotransmitters
-controlled substance!!!!!
-could be sedating; body will need to adjust to it

209
Q

topiramate (topamax)
-what kind of medication?
-what is it used for?
-SE
-when should this medication be avoided (what patient population?)

A

-HA medication
-prevention of seizures and prophylaxis for migraines
-weight loss
-avoid prescribing this med in pts with renal or hepatic issues or those with hx of eating disorder

210
Q

medications used to treat headaches (4)

A

topiramate (topamax)
betablockers
TCAs
“triptan”

211
Q

what medications are used to treat migraine headaches prophylactically?

A

topiramate (topamax)
betablockers
TCA’s

212
Q

what medications are used to treat migraine headaches abortively?

A

“triptan” it sumatriptan (Imitrex)

213
Q

what is a good medication option to treat a patient’s migraines with a preexisting condition of depression?

A

TCA’s (prophylactically, though)

214
Q

what HA/migraine medication can cause increased risk of kidney stones?

A

topiramate (topamax)

215
Q

what HA/migraine medication should not be prescribed to those with a history of eating disorders?

A

topiramate (topamax)

216
Q

what HA/migraine medication should not be used in patients with hx of renal or hepatic issues?

A

topiramate (topamax)

217
Q

what HA/migraine medication is used to treat tension HA?

A

TCA’s

218
Q

when are prophylactic treatments utilized for migraines/HA?
why?

A

when patient takes abortive therapies >2x weekly.
-avoids rebound HA

219
Q

are all medications in the “triptan” class equivalent? explain.

A

NO!
-another medication from the same class can work for patient even if original med does not.

220
Q

what is the best abortive therapy for migraine HA?

A

“triptan” - sumatriptan

221
Q

what are the contraindications of “triptan” medications?

A

those with uncontrolled HTN; those with CV disease can worsen d/t vasoconstriction

222
Q

-when should abortive therapy be taken by pt?

A

as soon as HA begins

223
Q

what medication can help with cluster HA (abortive)?

A

intranasal or subQ sumatriptan
high flow O2 100% 7-15min
intranasal lidocaine

224
Q

what medication can help with cluster HA (prophylactic)?

A

CCB (verapamil)

225
Q

Levadopa-Carbidopa (Sinemet)
-what disease does this tx?
-why isn’t levadopa given by itself?
-when is this med administered during the disease process?
-what symptom does this treat best?
-adverse SE

A

-Parkinson’s disease
-levadopa given by itself is readily destroyed by the body; thus fairly large doses would be needed; when given with carbidopa, allows for lower dose of levodopa = less GI SE, too
-wait to initiate med until sx are interfering w/ quality of life
-bradykinesia
-hypotension

226
Q

Levadopa-Carbidopa (Sinemet)
-wear off phenomenon –> how long after starting med does this phenomenon tend to occur?

A

-w/i 5 years

227
Q

what is the first line treatment for Parkinson’s disease?

A

Levadopa-carbidopa

228
Q

how is Parkinson’s disease treated after the wearing off phenomenon occurs?

A

not much we can do

229
Q

Dopamine agonists
-example of med
-what is it used to treat?
-SE
-can it be used alongside Sinemet?

A

-ropinirole (requip), pramipexole (Mirapex)
-used to delay initiation of levadopa
-impulse control issues; leg edema (after initiation); issues with hypotension
-yes

230
Q

Meclizine
-what is meclizine (antivert) used to tx?
-what kind of medication is this?
-SE
-good choice of med for what patient population?
-advantages to this medication

A

-benign positional vertigo and labyrinthitis
-antiemetic
-mildly anticholinergic and sedative
-elderly population
-starts to work quickly; lasts for quite awhile in pts system

231
Q

Iron
-what process is iron necessary for?
-what kind of anemia occurs if iron stores are low?
-what are iron prescriptions based on?

A

-to make healthy and effective RBC
-iron deficiency anemia
-amount of elemental iron

232
Q

Iron
-what is the preferred version of iron used for supplementation?
-how long are iron-deficient patients treated?

A

-ferrous sulfate
-until pt has med goal lab values + at least 3-6 MO afterward

233
Q

Iron
-how should iron be ingested?
-things to consider/SE
-how is medication administered to peds patients

A

-on empty stomach and in acidic environment
-stay hydrated; may need stool softener and high fiber diet/commonly causes constipation
-administer with dropper (iron can stain teeth)

234
Q

Vitamin B12 - Cobalamin
-how is route chosen between oral or IM?
-what type of sx occur with vit B12 deficiency?

A

-choose route based on type of B12 deficiency anemia
-can lead to neurological sx; beefy red tongue

235
Q

what population common has a vit B12 deficiency?

A

vegans

236
Q

why does Pernicious anemia occur?

A

-lack of intrinsic factor in stomach needed to absorb oral vit B12

237
Q

is IM or oral vit B12 given to those with pernicious anemia?

A

IM (lacking intrinsic factor)

238
Q

should vegans receive oral or IM vit B12 if deficient?

A

oral for 6-12 week

239
Q

what vitamin can become depleted as a side effect of metformin use?

A

vit B12

S Michelle (18 decks)

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